"Spider Lamb Syndrome" or "hereditary chondrodysplasia" is a semi-lethal congenital disorder in sheep causing severe skeletal abnormalities. These abnormalities can include abnormally long, spider-like legs, humped and twisted spines, deformed ribs and sternebra, facial deformities, lack of body fat, and underdevelopment of muscle. The most severe lesions progress to compression fractures from mechanical stress due to abnormal limb angulation. Vanek et al. "Comparing spider syndrome in Hampshire and Suffolk sheep", Vet. Med., 82:430-437 (1987). Radiological evaluation of Spider lamb shoulders, elbows and sternum reveal multiple, irregular islands of ossification. Vanek et al. "Radiographic diagnosis of hereditary chondrodysplasia in newborn lambs", JAVMA, 194:244-248 (1989). Histologic examinations of the vertebrae and long bones indicate an increase in width of the zone of proliferation, as well as hypertrophy and unevenness of the growth cartilage. Chondrocytes appear vacuolated and disorganized, lining up in bent nonparallel columns. Rook et al. "Diagnosis of hereditary chondrodysplasia (spider lamb syndrome) in sheep", JAVMA, 188:713-718 (1988), Troyer et al. "A morphologic and biochemical evaluation of the spider syndrome in Suffolk sheep", Anat. Histol. Embryol., 17:289-300 (1988). However, there are no deformities in the chondrocyte organelles (Troyer et al., 1988), suggesting that no problem exists with structural components of the cells themselves. Also, no chromosomal abnormalities can be found in Spider lambs. Vanek et al. "Comparison of G-banded chromosomes from clinically normal lambs and lambs affected with ovine hereditary chondrodysplasia (spider syndrome)", Am J. Vet. Res., 49:1164-1168 (1988).
Spider lamb Syndrome was first identified in newborn black-faced lambs during the mid-1970's. The syndrome has since surfaced in several sheep breeds in the United States and Canada within the last two decades. Such sheep breeds, include, but are not limited to, North American Suffolks and Hampshires, and United States Southdowns, Oxfords and Shropshires. In addition, cases of Spider Lab Syndrome have been reported in New Zealand and Australia, after the importation of several United States Suffolk rams into Australia in the early 1990's. It is believed this disorder arose as a mutation in a Suffolk genetic line that was used heavily during the late 1960's because of desirable production and show-ring characteristics.
Breeding studies have established that the gene responsible for this disease has an autosomal recessive mode of inheritance. Thomas and Cobb, "Spider syndrome and other genetic defects'", Sheep Mag. 7:44-46 (1986); Berg et al. "The mode of inheritance of the `Spider` Lamb Syndrome in Suffolk sheep", SID Res. Digest 4:1-3 (1987); Vanek et al., (1989). Thus, animals with two copies of the normal form (allele) of the gene are normal in appearance (homozygous normal or "NN") as are, most often, animals with one copy of the normal allele and one copy of the Spider Lamb Syndrome ("SLS") allele (heterozygous normal or "NS") . However, the homozygous normal animal can never produce a Spider offspring whereas the heterozygous or carrier animal has about 25% Spider offspring if mated to another carrier. Those animals with two copies of the SLS allele have the Spider phenotype and are rarely used for breeding purposes. While dramatic culling of all suspected carriers would reduce the frequency of the gene, it is a long and very expensive process. Progeny testing of potential breeding rams is another method of reducing gene frequency but it is also costly.
Due to SLS's recessive nature, it would be a significant improvement in the art to have a diagnostic or genetic screening test to determine, for example, whether or not a sheep is a carrier of the gene for SLS.